Literature DB >> 8513123

Lesion-induced NADPH-diaphorase reactivity in neocortical pyramidal neurones.

P D Kitchener1, C E Van der Zee, J Diamond.   

Abstract

Pyramidal neurones of the rat neocortex do not normally express NADPH-diaphorase reactivity. However, after stab lesions which extended through the entire depth of the neocortex, strong NADPH-diaphorase reactivity was observed in pyramidal neurones at 7 and 14 days post-lesion. At 3 and 21 days post-lesion fewer and less reactive pyramidal neurones were observed, and no reactive pyramidal neurones were seen at 2 and 26 days post-lesion. The great majority of reactive pyramidal neurones were in layers V and VI and most were situated medial to the lesion. The induction of NADPH-diaphorase implies that the capability to synthesize nitric oxide may be a component of the pyramidal neurones' response to traumatic injury.

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8513123     DOI: 10.1097/00001756-199305000-00006

Source DB:  PubMed          Journal:  Neuroreport        ISSN: 0959-4965            Impact factor:   1.837


  4 in total

Review 1.  NO as a signalling molecule in the nervous system.

Authors:  Juan V Esplugues
Journal:  Br J Pharmacol       Date:  2002-03       Impact factor: 8.739

Review 2.  Regulation of gap junction coupling in the developing neocortex.

Authors:  B Rörig; B Sutor
Journal:  Mol Neurobiol       Date:  1996-06       Impact factor: 5.590

Review 3.  Free radicals as mediators of neuronal injury.

Authors:  F Facchinetti; V L Dawson; T M Dawson
Journal:  Cell Mol Neurobiol       Date:  1998-12       Impact factor: 5.046

4.  In the hippocampus in vivo, nitric oxide does not appear to function as an endogenous antiepileptic agent.

Authors:  J L Stringer; F Erden
Journal:  Exp Brain Res       Date:  1995       Impact factor: 1.972

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.